Evidence map›Paper›PMID 32160773›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2020

Myristoylation of LMCD1 Leads to Its Species-Specific Derepression of E2F1 and NFATc1 in the Modulation of CDC6 and IL-33 Expression During Development of Vascular Lesions.

Suresh Govatati, Prahalathan Pichavaram, Jagadeesh Janjanam, Liang Guo, Renu Virmani, Gadiparthi N Rao

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. The Paradigm Change of IL-33 in Vascular Biology.International journal of molecular sciences · 2021
    Review
  8. Review
  9. Article
  10. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Suresh GovatatiFrom the Department of Physiology, University of Tennessee Health Science Center, Memphis (S.G., P.P., J.J., G.N.R.).
Prahalathan PichavaramFrom the Department of Physiology, University of Tennessee Health Science Center, Memphis (S.G., P.P., J.J., G.N.R.).
Jagadeesh JanjanamFrom the Department of Physiology, University of Tennessee Health Science Center, Memphis (S.G., P.P., J.J., G.N.R.).
Liang GuoCVPath Institute, Inc, Gaithersburg, MD (L.G., R.V.).
Renu VirmaniCVPath Institute, Inc, Gaithersburg, MD (L.G., R.V.).
Gadiparthi N RaoFrom the Department of Physiology, University of Tennessee Health Science Center, Memphis (S.G., P.P., J.J., G.N.R.).
University of Tennessee Health Science Center · US

Funding

NFATs AND VASCULAR INJURYR01HL069908 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI RAO, GADIPARTHI N · 2002 to 2019
$5.9M
GPCR Signaling & Vascular Wall RemodelingR01HL103575 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI RAO, GADIPARTHI N · 2011 to 2019
$4.1M
NHLBI NIH HHS R01 HL069908NHLBI NIH HHS R01 HL103575
6 · The paper itself

Abstract

objectiveIn view of our previous observations on differential expression of LMCD1 (LIM and cysteine-rich domains 1) in human versus rodents, we asked the question whether LMCD1 plays a species-specific role in the development of vascular lesions. Approach and Results: A combination of genetic, molecular, cellular, and disease models were used to test species-specific role of LMCD1 in the pathogenesis of vascular lesions. Here, we report species-specific regulation of LMCD1 expression in mediating vascular smooth muscle cell proliferation and migration during vascular wall remodeling in humans versus mice. Thrombin induced LMCD1 expression in human aortic smooth muscle cells but not mouse aortic smooth muscle cells via activation of Par1 (protease-activated receptor 1)-Gαq/11 (Gα protein q/11)-PLCβ3 (phospholipase Cβ3)-NFATc1 (nuclear factor of activated T cells 1) signaling. Furthermore, although LMCD1 mediates thrombin-induced proliferation and migration of both human aortic smooth muscle cells and mouse aortic smooth muscle cells via influencing E2F1 (E2F transcription factor 1)-mediated CDC6 (cell division cycle 6) expression and NFATc1-mediated IL (interleukin)-33 expression, respectively, in humans, it acts as an activator, and in mice, it acts as a repressor of these transcriptional factors. Interestingly, LMCD1 repressor activity was nullified by N-myristoyltransferase 2-mediated myristoylation in mouse. Besides, we found increased expression of LMCD1 in human stenotic arteries as compared to nonstenotic arteries. On the other hand, LMCD1 expression was decreased in neointimal lesions of mouse injured arteries as compared to noninjured arteries.

conclusionsTogether, these observations reveal that LMCD1 acts as an activator and repressor of E2F1 and NFATc1 in humans and mice, respectively, in the induction of CDC6 and IL-33 expression during development of vascular lesions. Based on these findings, LMCD could be a potential target for drug development against restenosis and atherosclerosis in humans.

Indexed as

Vascular RemodelingAnimalsCell Cycle ProteinsCell MovementCell ProliferationCells, CulturedCo-Repressor ProteinsDisease Models, AnimalE2F1 Transcription FactorFemaleGene Expression RegulationHumansInterleukin-33LIM Domain ProteinsMaleMice, Inbred C57BLCDC6 protein, humanCDC6 protein, mouseCell Cycle ProteinsCo-Repressor ProteinsE2F1 protein, humanE2f1 protein, mouseE2F1 Transcription FactorIL33 protein, humanIl33 protein, mouseInterleukin-33LIM Domain ProteinsLMCD1 protein, humanLmcd1 protein, mouseMyristic AcidNFATC1 protein, humanNfatc1 protein, mouseNFATC Transcription FactorsNuclear ProteinsThrombinatherosclerosishumansinterleukinmicethrombin

Identifiers

PMID32160773
PMCPMC7180120
OpenAlexW3012124317

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.